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Article
Nature Neuroscience  1, 69 - 73 (1998)
doi:10.1038/271

Cortisol levels during human aging predict hippocampal atrophy and memory deficits

Sonia J. Lupien1, 2, Mony de Leon3, Susan de Santi3, Antonio Convit3, Chaim Tarshish3, N. P. V. Nair1, Mira Thakur1, Bruce S. McEwen4, Richard L. Hauger5 & Michael J. Meaney1

1  Aging Research Program, Douglas Hospital Research Center, Department of Psychiatry, McGill University, 6875 Boulevard Lasalle, Verdun (Québec), H4H-1R3, Canada

2  Human Psychoneuroendocrine Research Laboratory, Geriatric Institute of Montreal, 4565 Queen Mary, Montreal (Québec) H3W-1W5, Canada

3  Aging and Dementia Research Center, NY University Medical Center, 550 First Avenue, New York, New York 10016, USA

4  Laboratory of Neuroendocrinology, Rockefeller University, 1230 York Avenue, New York, New York 10021, USA

5  Department of Psychiatry, University of California and VA Medical Center, 3350 La Jolla Village Drive, San Diego, California 92161, USA

Correspondence should be addressed to Sonia J. Lupien lupiens@magellan.umontreal.ca
Elevated glucocorticoid levels produce hippocampal dysfunction and correlate with individual deficits in spatial learning in aged rats. Previously we related persistent cortisol increases to memory impairments in elderly humans studied over five years. Here we demonstrate that aged humans with significant prolonged cortisol elevations showed reduced hippocampal volume and deficits in hippocampus-dependent memory tasks compared to normal-cortisol controls. Moreover, the degree of hippocampal atrophy correlated strongly with both the degree of cortisol elevation over time and current basal cortisol levels. Therefore, basal cortisol elevation may cause hippocampal damage and impair hippocampus-dependent learning and memory in humans.

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Nature Neuroscience
ISSN: 1097-6256
EISSN: 1546-1726
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